Elsevier

The Spine Journal

Volume 6, Issue 6, Supplement, November–December 2006, Pages S190-S197
The Spine Journal

Review Article
Pathophysiology of cervical myelopathy

https://doi.org/10.1016/j.spinee.2006.04.024Get rights and content

Abstract

Background content

Cervical myelopathy is a group of closely related disorders usually caused by spondylosis or by ossification of the posterior longitudinal ligament and is characterized by compression of the cervical spinal cord or nerve roots by varying degrees and number of levels. The decrease in diameter of the vertebral canal secondary to disc degeneration and osteophytic spurs compresses the spinal cord and nerve roots at one or several levels, producing direct damage and often secondary ischemic changes.

Purpose

Clinicians who treat cervical myelopathy cord injuries should have a basic understanding of the pathophysiology and the processes that are initiated after the spinal cord has been injured.

Study design/setting

Literature review.

Methods

Literature review of human cervical myelopathy and clinically relevant animal models to further our understanding of the pathological mechanisms involved.

Results

The pathophysiology of cervical myelopathy involves static factors, which result in acquired or developmental stenosis of the cervical canal and dynamic factors, which involve repetitive injury to the cervical cord. These mechanical factors in turn result in direct injury to neurons and glia as well as a secondary cascade of events including ischemia, excitotoxicity, and apoptosis; a pathobiology similar to that occurring in traumatic spinal cord injury.

Conclusions

This review summarizes some of the significant pathophysiological processes involved in cervical myelopathy.

Introduction

Cervical myelopathy is the most serious condition of cervical spondylosis and is the most commonly acquired cause of spinal cord dysfunction among those aged over 55 years [1]. This disorder was originally described by Stookey in 1928 and was attributed to compression of the cord by cartilaginous nodules of degenerated disc material [2]. The symptoms and signs with which myelopathy patients present are dependent on the relative degree to which the posterior, dorsolateral and ventrolateral columns, the ventral horns, and the cervical nerve root of the spinal cord are involved [3]. In most cases, patients present with more than one of the aforementioned structures being affected [4].

Although the exact pathophysiology underlying cervical myelopathy remains uncertain, it is largely accepted to be a disorder that involves compressive forces on the spine, likely due to multiple factors. Cervical cord compression can occur as a result of a disc herniation alone; degenerative changes that occur in the spine such as degeneration of the joints, intervertebral discs, ligaments, and connective tissue of the cervical vertebrae; and bone spur growth in the spinal canal (spondylosis). Posteriorly, infolding of the ligamentum flavum and facet joint capsule can create decreased space within the spinal canal and foraminal dimensions [5]. Conversely one is placed at increased risk for developing cervical cord compression and myelopathy as the space within the spinal canal narrows (stenosis).

Section snippets

Pathogenesis of cervical myelopathy

The pathophysiology of cervical myelopathy involves static factors, which result in acquired or developmental stenosis of the cervical canal, and dynamic factors, which involve repetitive injury to the cervical cord. These mechanical factors in turn result in direct injury to neurons and glia as well as a secondary cascade of events including ischemia, excitotoxicity, and apoptosis (Table 1). Indeed, the pathobiology of cervical myelopathy bears many similarities to traumatic spinal cord injury

Acquired spinal stenosis—Spondylosis and disc degeneration

In healthy adults, the intervertebral discs in the cervical spine have a structure analogous to that of the discs of the lumbar spine, consisting of the annulus fibrosis and nucleus pulposus [7]. The chemical composition of the nucleus pulposus and annulus fibrosis deteriorates with age [5]. This results in a progressive loss of viscoelastic properties of the spinal cord and disc bulging. However, it has been observed that in the first and second decades of life, before complete ossification

Congenital spinal canal stenosis

Numerous observational studies demonstrate that congenital or developmental stenosis of the cervical spinal canal is highly correlated with the later development of cervical myelopathy. A number of authors have identified the normal sagittal diameter of the spinal canal is approximately 17–18 mm between C3 and C7 [37], [38], [39], [40]. Conversely, patients with a sagittal spinal canal <13 mm in diameter are at high risk for developing signs and symptoms of myelopathy [41].

Mechanistically, a

Stenosis via dynamic mechanical factors

Penning demonstrated that cervical myelopathy is strongly suspected when the dynamic canal space during extremes of flexion or extension is <11 mm [37]. Dynamic hyperextension of the neck narrows the spinal canal by shingling the laminae and buckling the ligamentum flavum [5]. Translation and angulation between vertebral bodies in flexion-extension can also transiently narrow the canal. Moreover, in conjunction with a preexisting stenosis there is increased strain and shear forces applied on

Stretch-associated forces applied to spinal cord axons

During normal flexion of the spinal column, axial strain results from the elongation of the spinal canal and stretching of the spinal cord [43]. The idea that increased axial strain after neck elongation can be potentially detrimental to the health of the cervical spinal cord has been suggested for over 30 years [46], [47]. Bilston and Thibault used isolated cervical spinal cord samples obtained from cadavers at autopsy to investigate axial tension at applied physiological strain rates achieved

Ischemia

Considerable evidence exists to support ischemia as a major underlying pathologic event, which contributes to the etiology of myelopathy. Anterior compression compromises perfusion through the transverse arterioles arising from the anterior sulcal arteries, while posterior cord compression works to reduce perfusion to the intramedullary branches of the central gray matter [50]. One cell type now known to be hypersensitive to ischemic injury is the oligodendrocyte [51]. These cells are chiefly

Apoptosis

Apoptosis is a morphologically defined form of programmed cell death seen in a variety of circumstances, including immune cell selection and development. Apoptosis has very recently been seen after ischemic or traumatic injury to the central nervous system, suggesting that active cell death as well as passive necrosis may mediate damage after central nervous system injury. Several investigators now report that secondary apoptotic cell death occurs after acute traumatic spinal cord injury in

Conclusion

In conclusion, the pathophysiology of cervical myelopathy involves the combination of mechanical induced static and dynamic factors which trigger a complex cascade of biomolecular changes including ischemia, excitotoxicity, and apoptosis. Further research is required to elucidate the mechanisms underlying progressive cell death in cervical myelopathy. With an increased understanding of the pathophysiological mechanisms involved in cervical myelopathy, there will be improved reparative and

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